Deficiency of Histone Methyltransferase SET Domain‐Containing 2 in Liver Leads to Abnormal Lipid Metabolism and HCC

• Published in: Hepatology (Baltimore, Md.) Vol. 73; no. 5; pp. 1797 - 1815
• Main Authors: Li, Xue‐Jing, Li, Qing‐Lan, Ju, Lin‐Gao, Zhao, Chen, Zhao, Lan‐Shen, Du, Jia‐Wen, Wang, Yan, Zheng, Ling, Song, Bao‐Liang, Li, Lian‐Yun, Li, Li, Wu, Min
• Format: Journal Article
• Language: English
• Published: United States Wolters Kluwer Health, Inc 01.05.2021
• Subjects: Activator protein 1; Alanine Transaminase - blood; Animals; Aspartate Aminotransferases - blood; Carcinoma, Hepatocellular - etiology; Carcinoma, Hepatocellular - metabolism; Cell Line, Tumor; Cholesterol; Cholesterol - blood; Chromatin; Chromatin Immunoprecipitation; CRISPR-Associated Protein 9; CRISPR-Cas Systems; Diethylnitrosamine; DNA damage; Epigenetics; Gene Editing; Gene Expression Regulation, Neoplastic; HEK293 Cells; Hep G2 Cells; Hepatology; High fat diet; Histone methyltransferase; Histone-Lysine N-Methyltransferase - deficiency; Histone-Lysine N-Methyltransferase - metabolism; Homeostasis; Humans; Immunoprecipitation; Lipid Metabolism; Lipids; Liver; Liver - metabolism; Liver Neoplasms - etiology; Liver Neoplasms - metabolism; Male; Metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; p53 Protein; Sequence analysis; Triglycerides - blood; Tumor suppressor genes

Background and Aims Trimethylation of Lys36 on histone 3 (H3K36me3) catalyzed by histone methyltransferase SET domain‐containing 2 (SETD2) is one of the most conserved epigenetic marks from yeast to mammals. SETD2 is frequently mutated in multiple cancers and acts as a tumor suppressor. Approach and...